| http://purl.uniprot.org/citations/21250838 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/21250838 | http://www.w3.org/2000/01/rdf-schema#comment | "B lymphocyte stimulator (BLyS) and APRoliferation inducing ligand (APRIL) are members of the TNF superfamily that regulate B-cell survival and autoreactivity. To further understand the significance of elevated BLyS and APRIL in systemic lupus erythematosus (SLE), we examined the expression profiles of their receptors (B-cell-activating factor (BAFF)-R, transmembrane activator and calcium modulator and cyclophilin ligand interactor, and B cell maturation antigen (BCMA)) on B-cell subsets in SLE and also investigated the differential expression and function of BCMA in TLR9-induced B-cell activation. While BAFF-R expression on SLE B cells was significantly lower compared to healthy control B cells (p = 0.003), BCMA expression was substantially higher on SLE B cells (p = 0.038), especially on memory cells and plasmablasts. BCMA(+) cells had higher CD19 and CD86 expression, indicating a greater degree of activation in both healthy and lupus patients. CpG stimulation increased BCMA expression on B cells and induced the proliferation and maturation of BCMA(+) B cells. A BCMA agonistic antibody also enhanced CpG-induced proliferation, activation, and IgG secretion by B cells in both healthy controls and lupus patients. Furthermore, the agonistic BCMA antibody co-stimulated auto-antibody production by CpG-stimulated lupus B cells in vitro. Signaling through BCMA enhances B cell activation following exposure to TLR9 agonists, and increased expression in SLE may contribute to the production of IgG autoantibodies."xsd:string |
| http://purl.uniprot.org/citations/21250838 | http://purl.org/dc/terms/identifier | "doi:10.3109/08916934.2010.509122"xsd:string |
| http://purl.uniprot.org/citations/21250838 | http://purl.uniprot.org/core/author | "Kim J."xsd:string |
| http://purl.uniprot.org/citations/21250838 | http://purl.uniprot.org/core/author | "Elkon K.B."xsd:string |
| http://purl.uniprot.org/citations/21250838 | http://purl.uniprot.org/core/author | "Min J.K."xsd:string |
| http://purl.uniprot.org/citations/21250838 | http://purl.uniprot.org/core/author | "Gross J.A."xsd:string |
| http://purl.uniprot.org/citations/21250838 | http://purl.uniprot.org/core/author | "Dillon S.R."xsd:string |
| http://purl.uniprot.org/citations/21250838 | http://purl.uniprot.org/core/date | "2011"xsd:gYear |
| http://purl.uniprot.org/citations/21250838 | http://purl.uniprot.org/core/name | "Autoimmunity"xsd:string |
| http://purl.uniprot.org/citations/21250838 | http://purl.uniprot.org/core/pages | "69-81"xsd:string |
| http://purl.uniprot.org/citations/21250838 | http://purl.uniprot.org/core/title | "Increased BCMA expression in lupus marks activated B cells, and BCMA receptor engagement enhances the response to TLR9 stimulation."xsd:string |
| http://purl.uniprot.org/citations/21250838 | http://purl.uniprot.org/core/volume | "44"xsd:string |
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